Gastritis is believed to affect about half of people worldwide.[5] In 2013 there were approximately 90 million new cases of the condition.[8] As people get older the disease becomes more common.[5] It, along with a similar condition in the first part of the intestines known as duodenitis, resulted in 60,000 deaths in 2013.[9]H. pylori was first discovered in 1981 by Barry Marshall and Robin Warren.[10]

Many people with gastritis experience no symptoms at all. However, upper centralabdominal pain is the most common symptom; the pain may be dull, vague, burning, aching, gnawing, sore, or sharp.[11] Pain is usually located in the upper central portion of the abdomen,[12] but it may occur anywhere from the upper left portion of the abdomen around to the back.

Helicobacter pylori colonizes the stomachs of more than half of the world's population, and the infection continues to play a key role in the pathogenesis of a number of gastroduodenal diseases. Colonization of the gastric mucosa with Helicobacter pylori results in the development of chronic gastritis in infected individuals, and in a subset of patients chronic gastritis progresses to complications (e.g., ulcer disease, gastric neoplasias, some distinct extragastric disorders).[13] However, over 80 percent of individuals infected with the bacterium are asymptomatic and it has been postulated that it may play an important role in the natural stomach ecology.[14]

Gastritis may also develop after major surgery or traumatic injury ("Cushing ulcer"), burns ("Curling ulcer"), or severe infections. Gastritis may also occur in those who have had weight loss surgery resulting in the banding or reconstruction of the digestive tract.

Acute erosive gastritis typically involves discrete foci of surface necrosis due to damage to mucosal defenses.[16] NSAIDs inhibit cyclooxygenase-1, or COX-1, an enzyme responsible for the biosynthesis of eicosanoids in the stomach, which increases the possibility of peptic ulcers forming.[17] Also, NSAIDs, such as aspirin, reduce a substance that protects the stomach called prostaglandin. These drugs used in a short period are not typically dangerous. However, regular use can lead to gastritis.[18] Additionally, severe physiologic stress ("stress ulcers") from sepsis, hypoxia, trauma, or surgery, is also a common etiology for acute erosive gastritis. This form of gastritis can occur in more than 5% of hospitalized patients.

Also, note that alcohol consumption does not cause chronic gastritis. It does, however, erode the mucosal lining of the stomach; low doses of alcohol stimulate hydrochloric acid secretion. High doses of alcohol do not stimulate secretion of acid.[19]

Chronic gastritis refers to a wide range of problems of the gastric tissues.[16] The immune system makes proteins and antibodies that fight infections in the body to maintain a homeostatic condition. In some disorders the body targets the stomach as if it were a foreign protein or pathogen; it makes antibodies against, severely damages, and may even destroy the stomach or its lining.[18] In some cases bile, normally used to aid digestion in the small intestine, will enter through the pyloric valve of the stomach if it has been removed during surgery or does not work properly, also leading to gastritis. Gastritis may also be caused by other medical conditions, including HIV/AIDS, Crohn's disease, certain connective tissue disorders, and liver or kidney failure. Since 1992, chronic gastritis lesions are classified according to the Sydney system.[20]

Mucous gland metaplasia, the reversible replacement of differentiated cells, occurs in the setting of severe damage of the gastric glands, which then waste away (atrophic gastritis) and are progressively replaced by mucous glands. Gastric ulcers may develop; it is unclear if they are the causes or the consequences. Intestinal metaplasia typically begins in response to chronic mucosal injury in the antrum, and may extend to the body. Gastric mucosa cells change to resemble intestinal mucosa and may even assume absorptive characteristics. Intestinal metaplasia is classified histologically as complete or incomplete. With complete metaplasia, gastric mucosa is completely transformed into small-bowel mucosa, both histologically and functionally, with the ability to absorb nutrients and secrete peptides. In incomplete metaplasia, the epithelium assumes a histologic appearance closer to that of the large intestine and frequently exhibits dysplasia.[16]

Cytoprotective agents are designed to help protect the tissues that line the stomach and small intestine. They include the medications sucralfate and misoprostol. If NSAIDs are being taken regularly, one of these medications to protect the stomach may also be taken. Another cytoprotective agent is bismuth subsalicylate.

Several regimens are used to treat H. pylori infection. Most use a combination of two antibiotics and a proton pump inhibitor. Sometimes bismuth is also added to the regimen.